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    Have Researchers Finally Figured Out Crohn's Disease?


    Jefferson Adams
    Image Caption: Photo: CC--Bilal Kamoon

    Celiac.com 10/24/2016 - A team of researchers led by Mahmoud A Ghannoum, PhD, professor and director of the Center for Medical Mycology at Case Western Reserve and University Hospitals Cleveland Medical Center, has made a breakthrough in understanding Crohn's disease.


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    The researchers were the first to document the role of a fungus in the human gut as playing a major role in Crohn's disease. As part of their efforts, their research team assessed the mycobiome and bacteriome of patients with Crohn's disease, their Crohn's-free first degree relatives in 9 families in northern France and Belgium, and in Crohn's-free individuals from 4 families in the same region.

    For their study, the team analyzed fecal samples from 20 Crohn's patients, and from 28 Crohn's-free patients from nine families, and of 21 Crohn's-free patients from four nearby families. The team found that people with Crohn's disease showed strong fungal-bacterial interaction. Specifically, in Crohn's, two bacteria, Escherichia coli and Serratia marcescens, acted in unison with the fungus Candida tropicalis.

    Family members with Crohn's showed substantially higher numbers of all three microbes, as compared to their healthy relatives, suggesting co-action between the bacteria and fungus in the gut. The team's lab tests confirmed that the three work together by E. coli cells fusing to the fungal cells, while S. marcescens acts as a bridge to connect the microbes. This produces what is called a biofilm, a thin, slimy layer of microorganisms that, among other things, coats part of the intestinal tract, triggering the inflammation seen in Crohn's disease.

    Researchers had previously found the fungus in mice with Crohn's, but this is the first time any fungus has been linked to Crohn's in humans. The study is also the first to document S. marcescens as a main factor in Crohn's.

    The team also found that Crohn's patients suffer from substantially reduced numbers of beneficial bacteria, which corroborated earlier study findings. These findings could lead to helpful new treatment approaches to the traditionally stubborn condition that is Crohn's disease.

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    Scott Adams
    In the Friday, February 9, 1996 edition of the Independent newspaper (UK), there was a short article reporting research into ME (myalgic encephalomyelitis) by doctors at the Royal Hallamshire Hospital in Sheffield. Their research was published that same weeks Lancet.
    Mysterious symptoms, including muscle weakness, wasting, and poor coordination and balance may be due to an undiagnosed allergy to wheat, barley, oats or rye, according to new research which may have implications for some people with ME...A study of 53 patients with these and other unexplained neurological symptoms, found that nearly three-fifths of them had antibodies to gluten in their blood...none of the patients in the Sheffield group had been diagnosed with celiac disease but when samples of tissue were removed from their gut, more than a third showed evidence of the disease or inflammation of the middle and lower gut.

    Scott Adams
    Celiac.com 01/10/2001 - According to the Food Standards Agency (FSA) of the UK, British health experts are exploring ways to eliminate a bacterium that has been linked to Crohns disease from the food chain. As reported by Reuters Health, scientists have warned of a widespread bacterium called Mycobacterium paratuberculosis that is the likely cause of the bowel disorder. This bacterium can survive the milks normal, or even prolonged pasteurization process.
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    Scott Adams
    Inflamm Bowel Dis. 2005 Jul;11(7):662-666. Celiac.com 06/30/2005 – Researchers in Italy have determined that those with Crohns disease also have a high prevalence of celiac disease. Their study evaluated 27 consecutive patients who were diagnosed with Crohns disease—13 were men and 14 were women, with a mean age of 32.3 years. Each patient was screened for celiac disease using antigliadin, antiendomysium, and antitransglutaminase blood antibody tests, and the sorbitol H2 breath test. If either the blood or breath test was positive, the patients were given a small bowel biopsy for final confirmation.
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    Jefferson Adams
    Celiac.com 02/18/2011 - In their search for a deeper understanding of the connections between celiac disease and Crohn’s disease, scientists have begun to focus on genetic variants that trigger inflammation in the gut.
    A research team examining associations between celiac disease and Crohn’s disease has now confirmed four common genetic variations between the two diseases.
    Their discovery may help to explain why people with celiac disease suffer Crohn’s disease at higher rates than the general population.
    Better understanding the genetic connections will likely pave the way for new treatments for symptoms common to both conditions, such as inflammation.
    The study used a new method of analysis called a genome-wide association study, or GWAS. This allows researchers to look at hundreds of thousands of genetic variations, called single nucleotide polymorphisms, or SNPs, that may be involved in any one disease.
    The research team compared 471,504 SNPs, representing the genomes of about 10,000 people, some of whom had Crohn’s disease, some of whom had celiac disease, and others who were healthy.
    They found four genes that seemed to raise the risk for both diseases. Two of these genes, IL18RAP and PTPN2, had already been associated with each disease.
    Another, called TAGAP, had previously been identified as a risk factor in celiac disease, but was newly associated with Crohn’s disease.
    The fourth gene, PUS10, had been previously been tied to Crohn’s disease, celiac disease, and ulcerative colitis.
    Three of the four genes seem to influence immune system response to perceived threats.
    “The first three we can say are involved in T-lymphocyte function,” Rioux says. “They seem to have a role to play in how these cells respond to a given stimulus.”
    In celiac disease, gluten-induced intestinal inflammation causes damage that prevents the intestine from absorbing nutrients in food. This can cause a wide range of problems, from anemia to osteoporosis to lactose intolerance.
    In Crohn’s disease, inflammation of the digestive tract often causes the bowel to empty frequently, resulting in diarrhea, among other problems.
    Some research shows that people with one condition are more likely to have the other. One study, for example, found that more than 18.5% of people with Crohn’s disease also have celiac disease.
    The study has “completely changed the way we can identify genetic risk factors,” says study co-author John D. Rioux, PhD, an associate professor of medicine at the University of Montreal, in Quebec, Canada.
    “There are sequence differences at the genetic level that get translated down to the protein levels,” Rioux notes. “And these differences may really nudge a person toward inflammation."
    He adds that "we’re just in the beginning, but we hope they may elucidate a common pathway and one day help us discover treatments that correct the underlying genetic changes.”
    Source:

    Jan. 27 issue of PLoS Genetics

  • Recent Articles

    Jefferson Adams
    Celiac.com 06/18/2018 - Celiac disease has been mainly associated with Caucasian populations in Northern Europe, and their descendants in other countries, but new scientific evidence is beginning to challenge that view. Still, the exact global prevalence of celiac disease remains unknown.  To get better data on that issue, a team of researchers recently conducted a comprehensive review and meta-analysis to get a reasonably accurate estimate the global prevalence of celiac disease. 
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    There are many reports in such journals connecting brain and neurological ailments with gluten, so it is not much of a stretch, on that basis alone, to suspect that stuttering may be a symptom of the gluten syndrome. Rodney Ford has even characterized celiac disease as an ailment that may begin through gluten-induced neurological damage (13) and Marios Hadjivassiliou and his group of neurologists and neurological investigators have devoted considerable time and effort to research that reveals gluten as an important factor in a majority of neurological diseases of unknown origin (14) which, as I have pointed out previously, includes most neurological ailments.
    My own experience with stuttering is limited. I stuttered as a child when I became nervous, upset, or self-conscious. Although I have been gluten free for many years, I haven’t noticed any impact on my inclination to stutter when upset. I don’t know if they are related, but I have also had challenges with speaking when distressed and I have noticed a substantial improvement in this area since removing gluten from my diet. Nonetheless, I have long wondered if there is a connection between gluten consumption and stuttering. Having done the research for this article, I would now encourage stutterers to try a gluten free diet for six months to see if it will reduce or eliminate their stutter. Meanwhile, I hope that some investigator out there will research this matter, publish her findings, and start the ball rolling toward getting some definitive answers to this question.
    Sources:
    1. Toft M, Dietrichs E. Aggravated stuttering following subthalamic deep brain stimulation in Parkinson’s disease--two cases. BMC Neurol. 2011 Apr 8;11:44.
    2. Tani T, Sakai Y. Stuttering after right cerebellar infarction: a case study. J Fluency Disord. 2010 Jun;35(2):141-5. Epub 2010 Mar 15.
    3. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    4. Jäncke L, Hänggi J, Steinmetz H. Morphological brain differences between adult stutterers and non-stutterers. BMC Neurol. 2004 Dec 10;4(1):23.
    5. Kell CA, Neumann K, von Kriegstein K, Posenenske C, von Gudenberg AW, Euler H, Giraud AL. How the brain repairs stuttering. Brain. 2009 Oct;132(Pt 10):2747-60. Epub 2009 Aug 26.
    6. Galantucci S, Tartaglia MC, Wilson SM, Henry ML, Filippi M, Agosta F, Dronkers NF, Henry RG, Ogar JM, Miller BL, Gorno-Tempini ML. White matter damage in primary progressive aphasias: a diffusion tensor tractography study. Brain. 2011 Jun 11.
    7. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    8. [No authors listed] Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 43-1988. A 52-year-old man with persistent watery diarrhea and aphasia. N Engl J Med. 1988 Oct 27;319(17):1139-48
    9. Molteni N, Bardella MT, Baldassarri AR, Bianchi PA. Celiac disease associated with epilepsy and intracranial calcifications: report of two patients. Am J Gastroenterol. 1988 Sep;83(9):992-4.
    10. http://ezinearticles.com/?Food-Allergy-and-Stuttering-Link&id=1235725 
    11. http://www.craig.copperleife.com/health/stuttering_allergies.htm 
    12. https://www.celiac.com/forums/topic/73362-any-help-is-appreciated/
    13. Ford RP. The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29.
    14. Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A. Does cryptic gluten sensitivity play a part in neurological illness? Lancet. 1996 Feb 10;347(8998):369-71.

    Jefferson Adams
    Celiac.com 06/14/2018 - Refractory celiac disease type II (RCDII) is a rare complication of celiac disease that has high death rates. To diagnose RCDII, doctors identify a clonal population of phenotypically aberrant intraepithelial lymphocytes (IELs). 
    However, researchers really don’t have much data regarding the frequency and significance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. Such data could provide useful comparison information for patients with RCDII, among other things.
    To that end, a research team recently set out to try to get some information about the frequency and importance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. The research team included Shafinaz Hussein, Tatyana Gindin, Stephen M Lagana, Carolina Arguelles-Grande, Suneeta Krishnareddy, Bachir Alobeid, Suzanne K Lewis, Mahesh M Mansukhani, Peter H R Green, and Govind Bhagat.
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    Repeat biopsy showed that the clonal or PCP pattern persisted for up to 2 years with no evidence of RCDII. The study indicates that better understanding of clonal T cell receptor gene rearrangements may help researchers improve refractory celiac diagnosis. 
    Source:
    Journal of Clinical Pathologyhttp://dx.doi.org/10.1136/jclinpath-2018-205023

    Jefferson Adams
    Celiac.com 06/13/2018 - There have been numerous reports that olmesartan, aka Benicar, seems to trigger sprue‐like enteropathy in many patients, but so far, studies have produced mixed results, and there really hasn’t been a rigorous study of the issue. A team of researchers recently set out to assess whether olmesartan is associated with a higher rate of enteropathy compared with other angiotensin II receptor blockers (ARBs).
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    After PS matching comparing olmesartan to other ARBs, hazard ratios were 1.21 (95% CI, 1.05‐1.40), 1.00 (95% CI, 0.88‐1.13), 1.22 (95% CI, 1.10‐1.36) and 1.04 (95% CI, 1.01‐1.07) for each outcome. Patients aged 65 years and older showed greater hazard ratios for celiac disease, as did patients receiving treatment for more than 1 year, and patients receiving higher cumulative olmesartan doses.
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    Source:
    Alimentary Pharmacology & Therapeutics